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EasySep™ Release人CD19 正选试剂盒

采用可解离磁珠技术的免疫磁珠正选

产品号 #(选择产品)

产品号 #17754_C

采用可解离磁珠技术的免疫磁珠正选

产品优势

  • 只需不到30分钟,分选出高纯度的人CD19+细胞
  • 无需洗涤去除EasySep™ Releasable RapidSpheres™可解离磁珠

产品组分包括

  • EasySep™ Release人CD19正选试剂盒(产品号 #17754)
    • EasySep™ Release人CD19正选抗体混合物,1 mL
    • EasySep™ Releasable RapidSpheres™ 50201磁珠,1 mL
    • EasySep™Release缓冲液(浓缩),3 x 1 mL
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总览

使用 EasySep™ Release人CD19正选试剂盒,可通过免疫磁性正选,轻松从新鲜或冻存的人外周血单个核细胞(PBMCs)及经洗涤的白细胞单采样本中分离出CD19+细胞。目的细胞用抗体和磁珠标记,并通过 EasySep™ 磁极进行无柱分选。非目的细胞通过简单倾倒弃去,而目的细胞则保留在试管中。随后,结合在使用EasySep™分离得到的CD19+细胞上的磁珠被解离,这些细胞可立即用于下游应用。使用该EasySep™ Release试剂盒分选之后,细胞表面仍结合有抗体复合物,并可能与Brilliant Violet™偶联的抗体、聚乙二醇修饰的蛋白质或其他化学相关配体相互作用。CD19抗原在成熟B细胞和祖B细胞表面表达,但在分化成熟为浆细胞时丢失。该抗原亦在滤泡树突状细胞表面表达。

磁体兼容性
• EasySep™ Magnet (Catalog #18000) • “The Big Easy” EasySep™ Magnet (Catalog #18001) • EasyPlate™ Magnet (Catalog #18102) • EasyEights™ Magnet (Catalog #18103)
 
亚型
细胞分选试剂盒
 
细胞类型
B 细胞
 
种属

 
样本来源
Leukapheresis,PBMC
 
筛选方法
Positive
 
品牌
EasySep
 
研究领域
免疫
 

实验数据

Starting with a single-cell suspension of human PBMCs, the CD19+ cell content of the isolated fraction is typically 97.7 ± 2.3% (mean ± SD using the purple EasySep™ Magnet). In the above example, the purities of the start and final isolated fractions are 6.2% and 98.0%, respectively.

产品说明书及文档

请在《产品说明书》中查找相关支持信息和使用说明,或浏览下方更多实验方案。

Document Type
Product Name
Catalog #
Lot #
Language
Catalog #
17754
Lot #
All
Language
English
Document Type
Safety Data Sheet 1
Catalog #
17754
Lot #
All
Language
English
Document Type
Safety Data Sheet 2
Catalog #
17754
Lot #
All
Language
English
Document Type
Safety Data Sheet 3
Catalog #
17754
Lot #
All
Language
English

应用领域

本产品专为以下研究领域设计,适用于工作流程中的高亮阶段。探索这些工作流程,了解更多我们为各研究领域提供的其他配套产品。

相关材料与文献

技术资料 (9)

文献 (3)

Leukemia-on-a-chip: Dissecting the chemoresistance mechanisms in B cell acute lymphoblastic leukemia bone marrow niche. C. Ma et al. Science advances 2020 oct

Abstract

B cell acute lymphoblastic leukemia (B-ALL) blasts hijack the bone marrow (BM) microenvironment to form chemoprotective leukemic BM niches facilitating chemoresistance and, ultimately, disease relapse. However, the ability to dissect these evolving, heterogeneous interactions among distinct B-ALL subtypes and their varying BM niches is limited with current in vivo methods. Here, we demonstrated an in vitro organotypic leukemia-on-a-chip" model to emulate the in vivo B-ALL BM pathology and comparatively studied the spatial and genetic heterogeneity of the BM niche in regulating B-ALL chemotherapy resistance. We revealed the heterogeneous chemoresistance mechanisms across various B-ALL cell lines and patient-derived samples. We showed that the leukemic perivascular endosteal and hematopoietic niche-derived factors maintain B-ALL survival and quiescence (e.g. CXCL12 cytokine signal VCAM-1/OPN adhesive signals and enhanced downstream leukemia-intrinsic NF-$\kappa$B pathway). Furthermore we demonstrated the preclinical use of our model to test niche-cotargeting regimens which may translate to patient-specific therapy screening and response prediction."
Fli1 Downregulation in Scleroderma Myeloid Cells Has Profibrotic and Proinflammatory Effects. A. M. Bujor et al. Frontiers in immunology 2020

Abstract

Scleroderma (SSc) is an autoimmune connective tissue disease characterized by immune dysregulation, vasculopathy, and fibrosis. We have previously demonstrated that low Fli1 expression in SSc fibroblasts and endothelial cells plays an important role in SSc pathogenesis. Cells of myeloid and lymphoid origin also express Fli1 and are dysregulated in patients with SSc, playing key roles in disease pathogenesis. However, the role for immune Fli1 in SSc is not yet clear. Our aim was to elucidate whether Fli1 contributes to the immune dysregulation seen in SSc. Comparison of the expression of Fli1 in monocytes, B- and T-cell fractions of PBMCs isolated from SSc patients and healthy controls (HC), showed an increase in Fli1 levels in monocytes. We used siRNA transfected human myeloid cells and mouse peritoneal macrophages obtained from Fli1 flox/flox LysMCre+/+ mice, and found that markers of alternative macrophage activation were increased with Fli1 deletion. Coculture of Fli1-deficient myeloid cells and primary human or mouse fibroblasts resulted in a potent induction of collagen type I, independent of TGF$\beta$ upregulation. We next analyzed global gene expression profile in response to Fli1 downregulation, to gain further insight into the molecular mechanisms of this process and to identify differentially expressed genes in myeloid cells. Of relevance to SSc, the top most upregulated pathways were hallmark IFN-$\gamma$ and IFN-$\alpha$ response. Additionally, several genes previously linked to SSc pathogenesis and fibrosis in general were also induced, including CCL2, CCL7, MMP12, and CXCL10. ANKRD1, a profibrotic transcription co-regulator was the top upregulated gene in our array. Our results show that Fli1-deficient myeloid cells share key features with cells from SSc patients, with higher expression of profibrotic markers and activation of interferon responsive genes, thus suggesting that dysregulation of Fli1 in myeloid cells may contribute to SSc pathogenesis.
CRISPR/Cas9-Correctable mutation-related molecular and physiological phenotypes in iPSC-derived Alzheimer's PSEN2 N141I neurons. M. Ortiz-Virumbrales et al. Acta neuropathologica communications 2017 dec

Abstract

Basal forebrain cholinergic neurons (BFCNs) are believed to be one of the first cell types to be affected in all forms of AD, and their dysfunction is clinically correlated with impaired short-term memory formation and retrieval. We present an optimized in vitro protocol to generate human BFCNs from iPSCs, using cell lines from presenilin 2 (PSEN2) mutation carriers and controls. As expected, cell lines harboring the PSEN2 N141I mutation displayed an increase in the A$\beta$42/40 in iPSC-derived BFCNs. Neurons derived from PSEN2 N141I lines generated fewer maximum number of spikes in response to a square depolarizing current injection. The height of the first action potential at rheobase current injection was also significantly decreased in PSEN2 N141I BFCNs. CRISPR/Cas9 correction of the PSEN2 point mutation abolished the electrophysiological deficit, restoring both the maximal number of spikes and spike height to the levels recorded in controls. Increased A$\beta$42/40 was also normalized following CRISPR/Cas-mediated correction of the PSEN2 N141I mutation. The genome editing data confirms the robust consistency of mutation-related changes in A$\beta$42/40 ratio while also showing a PSEN2-mutation-related alteration in electrophysiology.

更多信息

更多信息
种属 Human
Magnet Compatibility • EasySep™ Magnet (Catalog #18000) • “The Big Easy” EasySep™ Magnet (Catalog #18001) • EasyPlate™ Magnet (Catalog #18102) • EasyEights™ Magnet (Catalog #18103)
样本来源 Leukapheresis, PBMC
Selection Method Positive
标记抗体
质量保证:

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